The object of this work is the elucidation of the biochemical mechanism of compensatory skeletal muscle hypertrophy. These studies will give greater insight into the physiological regulation of normal and pathologic skeletal muscle metabolism and into the role of the nervous system in this regulation. They may also prove to be generalizable to the study of adaptation of other organs and tissues to increased physiological demand (e.g., the nervous system). We have found that Indomethacin inhibits the stretch-induced stimulation of protein synthesis in chick embryo muscle. This result suggests that prostaglandins may be involved in mediating the stretch response.